Biostatistical Analysis and Possible Forecasting of Relationship Between Uric Acid and Specific Laboratory Tests in Cases of Gouty Arthritis (original) (raw)
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The Korean journal of internal medicine, 2014
To investigate the rate of detection of monosodium urate (MSU) crystals in the synovial fluid (SF) of patients with acute gouty arthritis and factors associated with false-negative results. A total of 179 patients with acute gouty arthritis who had undergone SF crystal examination were identified from the data warehouse of two university hospitals. Clinical and laboratory data were obtained from the medical records. The overall rate of detection of MSU crystals was 78.8%. In univariate analyses, the only significant differences between the variables of crystal-negative and crystal-positive patients were a lower C-reactive protein level (p = 0.040) and fewer patients undergoing emergent surgery in the crystal-positive group (p = 4.5 × 10(-6)). In logistic regression analyses, MSU crystal-negative results were significantly associated with the interval from arthritis onset to crystal examination (p = 0.042), and this was the most significant risk factor for arthroscopic surgery (p = 2...
Annals of the Rheumatic Diseases, 2007
To determine whether hypouricaemic treatment results in the disappearance of urate crystals from gouty joints and to define the time required. Methods: In 18 patients with monosodium urate (MSU) crystal proven gout, and after the initiation of successful serum uric acid (SUA)-lowering treatment, an arthrocentesis of the asymptomatic signal joint (11 knees, 7 first metatarsophalangeal joints) was performed every 3 months to obtain a synovial fluid (SF) sample. The sample was then analysed for the presence of MSU crystals, and the number of crystals/4006 field was noted. SUA levels and the duration of gout were also noted. Results: MSU crystals disappeared from the SF of all 18 joints after reduction of SUA to normal levels. The time required for disappearance ranged from 3 to 33 months; disappearance time correlated with the duration of gout (r s = 0.71; p,0.01). The median number of MSU crystals in the SF samples before uratelowering treatment was 7.5 (2.5-11) crystals/4006 field, reducing to 3 (1-6.5) crystals/4006 field (p,0.05) at 3 months. Crystal counts continued to decrease after 3 months. Conclusions: In gout, reduction of SUA to normal levels results in disappearance of urate crystals from SF, requiring a longer time in those patients with gout of longer duration. This indicates that urate crystal deposition in joints is reversible. Normalisation of SUA levels results in a decrease in the concentration of MSU crystals in SF in the asymptomatic gouty joints. This may partially explain the reduced frequency of gouty attacks when a patient has been treated with SUA-lowering drugs.
Arthritis & rheumatology (Hoboken, N.J.), 2018
To estimate the prevalence and distribution of asymptomatic monosodium urate (MSU) crystal deposition in sons of people with gout. People with gout were mailed an explanatory letter enclosing a postage-paid study-pack to mail to their son(s) ≥20 years old. Sons interested in participating returned a reply-slip and underwent telephone screening. Subsequently they attended a study-visit for blood and urine collection, and musculoskeletal ultrasonography performed blind to serum urate (SU). Images were assessed for double contour sign (DCS), intra-articular or intra-tendinous aggregates/tophi, effusion and power Doppler. Logistic regression was used to examine associations. 131 sons (mean age 43.80 years, body mass index 27.10 kg/m ) completed assessments. 64.1% had SU ≥6 mg/dl, and 29.8% had either DCS or intra-articular aggregates/tophi in ≥1 joint. All participants with MSU deposition had involvement of either 1 metatarsophalangeal joint. 21.4% had intra-tendinous aggregates, and th...
Assessment of serum uric acid level among patients with rheumatoid arthritis
International Journal Of Community Medicine And Public Health, 2022
Background: Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily effects elderly population and commonly involves pain in the joints (the wrist and hands). Gout is a form of arthritis caused by excess uric acid in the blood stream, which can affect several joints. The co-occurrence of RA and gout in the same patient is rarely reported. The aim of this study was to assess the level of serum uric acid among patients with RA, and to observe any associations of serum uric acid levels with RA.Methods: In a descriptive cross-sectional study, a total of 70 blood samples were collected from patients. Anti-cyclic citrullinated peptide (anti-CCP) antibodies measured by ELISA method, serum C-reactive protein (CRP), Rheumatoid factor (RF) measured by latex agglutination test and serum uric acid levels measured with semi-autoanalyzer were carried out. Data was analyzed using a statistical package for social science for windows version 15.0. A p<0.05 was taken as level o...
The Journal of rheumatology, 2001
To determine if lowering of serum uric acid (SUA) concentrations below 6 mg/dl or longer duration of lowered SUA will result in depletion of urate crystals from the knee joints and prevent further attacks of gout. A prospective study was initiated 10 years ago at Philadelphia VA Medical Center to attempt to maintain SUA levels of patients with crystal proven gout at < 6.0 mg/dl. We recalled all 57 patients who were available during 1999. Patients were divided into 2 groups: Group A, with SUA still > 6 mg/dl, and Group B, with SUA < or = 6 mg/dl. A knee joint aspirate was requested from all asymptomatic Group B patients and many in Group A. Aspirates were examined by polarized light microscopy for identification of crystals. There were no differences between the groups in age, sex, duration of gout, or serum creatinine. Group A (n = 38) had a mean of 6 attacks of gout for the recent year, those with tophi having the most frequent attacks. Among the 16 patients in this group ...
New insights into the epidemiology of gout
Gout is a true crystal deposition disease caused by formation of monosodium urate crystals in joints and other tissues. It is a common inflammatory arthritis that has increased in prevalence in recent decades. Gout normally results from the interaction of genetic, constitutional and environmental risk factors. It is more common in men and strongly age related. A major determinant is the degree of elevation of uric acid levels above the saturation point for urate crystal formation, principally caused by inefficient renal urate excretion. Local joint tissue factors may influence the topography and extent of crystal deposition. Recent studies have provided information on dietary risk factors for gout: higher intakes of red meat, fructose and beer are independently associated with increased risk, whereas higher intakes of coffee, low-fat dairy products and vitamin C are associated with lower risk. Several renal urate transporters have been identified including URAT1 and SLC2A9 (GLUT9) and polymorphisms in these genes are associated with an increased risk of hyperuricaemia and gout. Many drugs influence serum uric acid levels through an effect on renal urate transport. Comorbidities, including the metabolic syndrome and impaired renal function are common in gout patients. The usual initial presentation of gout is with rapidly developing acute inflammatory monoarthritis, typically affecting the first MTP joint. If left untreated it may progress with recurrent acute attacks and eventual development of chronic symptoms and joint damage. New knowledge of the modifiable risk factors for gout can be integrated into the management strategy to optimize long-term patient outcomes.
Both gout and osteoarthritis (OA) are common forms of arthritis that inflict a huge burden to an aging population with the increasing prevalence of obesity. Clinicians have long observed the link between these two conditions. In this review, we summarize the evidence from epidemiologic and immunological studies that described the possible relationship between the two conditions. The recent new understanding on monosodium uric acid crystal-induced inflammation has given insight into probable shared pathogenesis pathways for both conditions. We describe the potential therapeutic implications, particularly regarding the possibility of repurposing traditional gout medications for use in OA.